[Collagen gastroenterocolitis]. / Une gastroentérocolite collagène.

INTRODUCTION: Collagenous gastroenterocolitis is a recently known rare cause of chronic diarrhoea, that raises numerous nosological and diagnostic problems. OBSERVATION: A 41 year-old woman was hospitalised for severe diarrhoea, diagnosed as collagenous gastroenterocolitis. Gastroscopy and ileocolonoscopy were macroscopically normal, but a 20 to 40 microns thick sub-epithelial collagenous band was revealed in the gastric, duodenal and colic biopsies. Parenteral nutrition and treatment with salazopyrine and prednisolone progressively normalised the transit. Three months later, only a 30 microns colic mucosa collagenous band persisted. All the biopsies taken during control gastro-colonoscopy 2 years later were histologically normal. After 5 years follow-up and absence of treatment, the patient no longer presented diarrhoea or biological abnormality. COMMENTS: This exceptional observation is a reminder that sub-epithelial collagen deposits are not always limited to the colon and therefore justify, in patients with collagenous colitis, systematic gastro-duodenal and ileum biopsies.

Effects of interferon-alpha on cytochrome P-450 isoforms 1A2 and 3A activities in patients with chronic hepatitis C.

BACKGROUND/AIM: The risk of adverse drug interactions with interferon-alpha has been poorly assessed. The aim of our study was to establish whether administration of interferon-alpha at therapeutic doses in patients with chronic hepatitis C may have significant inhibitory effects on other drug metabolism. The study was focused on cytochromes P-450 1A2 and 3A, two major isoforms involved in the metabolism of numerous substrates. METHODS: Eighteen patients with chronic active hepatitis C requiring an interferon-alpha treatment were studied. Cytochrome P-450 1A2 activity was determined on the basis of an in vivo caffeine metabolism study. Cytochrome P-450 3A activity was determined according to in vivo cortisol metabolism into 6-beta-hydroxycortisol. Both activities were determined 1 month before, at initiation and 1 month after interferon-alpha therapy (3 x 10(6) units, three times a week). RESULTS: There were no significant differences in the caffeine index (CYP 1A2) and in the 6-beta-hydroxycortisol/free cortisol urinary ratio (CYP 3A) before and after alpha interferon treatment CONCLUSION: Chronic administration of interferon-alpha at therapeutic doses does not change in vivo cytochrome P-450 1A2 and 3A activities. These results support the suggestion that drugs metabolized by these isoenzymes may be used together with interferon-alpha in patients with chronic hepatitis C without significant risks of drug interactions.

[Acute hepatitis due to ecstasy]. / Hépatite aiguë à l'ecstasy.

BACKGROUND: Ecstasy is a synthetic amphetamine which causes a wide variety of adverse effects. Hepatic toxicity was only recently demonstrated but can be quite severe. CASE REPORT: A 27-year-old male with no past medical or surgical history developed jaundice without fever. He was a regular user of ecstasy and had recently increased the number of doses consumed. No evidence of a viral, alcoholic, metabolic or autoimmune mechanism was found which could explain the hepatitis. Complete cure was obtained by discontinuing ecstasy. DISCUSSION: Few cases of ecstasy hepatic toxicity have been reported. Ecstasy was undoubtedly the causal agent in this case since other known causes of acute hepatitis were excluded, confirming the hepatotoxicity of ecstasy reported in the literature. The liver disease has been reported to range form acute regressive hepatitis to fatal liver failure. Iterative exposure can lead to fibrosis. The pathophysiological mechanism of this toxic effect is not well elucidated. Ischemia alone cannot explain all the clinical forms described, particularly cases without hyperpyrexia. Ecstasy must be added to the list of potential causes of acute hepatitis. Exposure must always be searched for in cases of acute hepatitis in young subjects.

[Hemostatic embolization of hepatocellular carcinoma with portal vein thrombosis complicated by hemoperitoneum]. / Embolisation hémostatique d'un carcinome hépatocellulaire avec thrombose de la veine porte compliqué d'un hémopéritoine.

A 59-year-old chronic drinker (120 g alcohol/day) was hospitalized for sudden increase in abdominal volume found to be caused by a hemoperitonoff resulting from ruptured hepatocellular carcinoma with thrombosis of the portal vein. Emergency arterial embolization with gelatin sponge successfully stopped intraperitoneal bleeding. No surgical treatment could be attempted due the severity of the cirrhosis. This patient survived for 4.5 month. Based on this observation and a review of the literature, it can be suggested that hemostatic embolization is an effective treatment for spontaneous hemorrhage of hepatocellular carcinoma even in cases with portal vein thrombosis.

[Post-traumatic thrombosis of the portal vein]. / Thrombose de la veine porte post-traumatique.

Blunt trauma to the abdomen is an exceptional cause of portal vein thrombosis. To our knowledge, 8 cases have been reported in the literature. When thrombosis of the portal vein occurs, a complete search for all the known main causes must be carried out before entertaining this diagnosis. Other causes may be cirrhosis, tumors and inflammation of the abdomen, coagulation disorders and hematologic diseases including latent myeloproliferative syndrome. We report a case in a 25-year-old man with an uneventful past history who presented with thrombosis of the portal vein after a violent blunt trauma which occurred during a rugby play. In this young man, none of the other potential causes was found, in particular bone marrow culture on medium with low growth-factor concentration allowed us to eliminate a latent myeloproliferative syndrome. The only triggering factor remaining was the recent abdominal trauma. After an 18-month follow-up, no other element has been observed which could have caused thrombosis of the portal vein.

Angiographic embolization of intrahepatic arterioportal fistula.

We report the case of a posttraumatic arteriovenous fistula between the right hepatic artery and the right portal vein remarkable in that clinical manifestations, including portal hypertension and mesenteric insufficiency findings, appeared latently and progressively worsened. This hepatoportal fistula was diagnosed by Doppler sonography and successfully treated by transcatheter embolization of feeding hepatic artery branch with steel coils. We emphasize the interest of pulsed Doppler in the diagnosis of hepatoportal fistula, in assessment of hemodynamic changes related to the fistula and in follow-up after treatment.

Tianeptine--an instance of drug-induced hepatotoxicity predicted by prospective experimental studies.

We report the case of a patient who developed acute hepatitis after taking tianeptine, a new tricyclic antidepressant, for 8 weeks. Hepatitis exhibited cholangitis-like clinical features and was associated with hypersensitivity manifestations suggestive of an immuno-allergic mechanism. Histological examination showed microvesicular steatosis. The discontinuation of tianeptine administration was followed by complete recovery. Immunoallergic hepatitis and microvesicular steatosis were predicted 2 years ago from prospective experimental studies prompted by the similarity of the chemical structures of tianeptine and amineptine, another tricyclic antidepressant, well-known for its hepatotoxicity. Experimentally, tianeptine has been found to be oxidized into reactive metabolites in several rodents and human liver and to produce microvesicular steatosis probably through inhibition of mitochondrial beta-oxidation of fatty acid in mice. This case illustrates the value of prospectively assessing potential hepatotoxicity mechanisms for new compounds chemically related to drugs already known to be hepatotoxic.